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Objective: We explored the mechanism of apoptosis in human esophageal cancer Eca109 cells by resveratrol. Methods: The suppressive ratio of resveratrol on Eca109 cells proliferation was evaluated by MTT colorimetric assay and morphology was observed by transmission electron microscope. The expression of survivin and bax was analyzed by RT-PCR and Flow Cytometry (FCM). Results: Resveratrol inhibited the growth of Eca109 cells in a dose-and time-dependent manner, and the suppressive ratio arrived at 76.42%. Morphological apoptosis could be observed after treated with resveratrol. The bulk of some drug-treated cells turned small and the nuclear chromatin became condensed and marginated. The results determined by RT-PCR and FCM showed that resveratrol could down-regulate surviving, while up-regulate bax. Conclusion: Resveratrol could induce the apoptosis of human esophageal cancer Eca109 cells, and its possible molecular mechanisms might be related to modulation the expression of survivin and bax.
Objective: We explored the mechanism of apoptosis in human esophageal cancer Eca109 cells by resveratrol. Methods: The suppressive ratio of resveratrol on Eca109 cells proliferation was evaluated by MTT colorimetric assay and morphology was observed by transmission electron microscope. The expression of survivin and bax was analyzed by RT-PCR and Flow Cytometry (FCM). Results: Resveratrol inhibited the growth of Eca109 cells in a dose-and time-dependent manner, and the suppressive ratio arrived at 76.42%. Morphological apoptosis could be observed after treatment with resveratrol. The bulk of some drug-treated cells turned small and the nuclear chromatin condensed and marginated. The results determined by RT-PCR and FCM showed that resveratrol could down-regulate surviving, while up-regulate bax. Conclusion: Resveratrol could induce the apoptosis of human esophageal cancer Eca109 cells, and its possible molecular mechanisms might be related to modulation the expression of survivin and bax.